So… big news. As of today, the Sweat Science blog is moving over to Runner’s World. All new posts will appear at runnersworld.com/sweat-science. It’s exciting news for me, and I think it’s good news for readers too, as I’ll explain below.

What will I find over at Runner’s World?
Don’t worry, it’s not turning into a running blog. In fact, the content will be exactly the same – the broad theme remains “the science of fitness,” encompassing everything from neuroscience to nutrition, with (I admit!) a particular focus on endurance sports. The blog won’t be going through any editorial process – no one from RW will be suggesting topics or overseeing what I write. (On the flip side, that means there will still be typos, unfortunately!)

Why move?
The move coincides with another career shift: starting in the April issue, I will be writing a monthly column in the print edition of Runner’s World, and will also become a contributing editor for the magazine. The column will be entirely separate from the Sweat Science blog; it’s called Fast Lane, and will focus on more applied training ideas for serious runners.

No, really… why?
Hey, let’s be honest: the other part of the reason is money. I’ll now be able to make part of my living from this blog – which is why I think the move is good news for readers. Sweat Science has grown far beyond what I anticipated when I started it three years ago, and now takes up a considerable amount of time. I’ve resisted accepting advertising and making quid pro quo arrangements, in part because I’m not confident that I’d manage to say what I really think about fitness products and research if I’m also accepting money or free stuff from the people selling them. Getting a paycheque from Runner’s World allows me to keep spending time reading and dissecting the literature without establishing direct relationships with advertisers whose products I write about. (Yes, I realize that RW will have ads from, for example, shoe companies – but the extra degree of separation makes a big difference to me.)

Paycheque?
Oh yeah, I guess I’ll probably have to switch to American spelling. So maybe I am a sell-out after all…

What now?
I hope you’ll update your bookmarks, browsing habits, RSS feeds, and whatever other newfangled social media tools bring you to this site. As I’ve mentioned elsewhere, this blog has changed my own practice of journalism for the better: by the time I write about a neat new piece of research for a newspaper or magazine these days, chances are I’ve been directed to an interesting new angle or a relevant counterargument by someone in the comments section of the blog. I sincerely appreciate all those contributions, and hope they’ll continue.

An odd little study from researchers at UCLA, just published in PLoS ONE (full text here; press release here) looks at how alcohol extends lifespan in worms. In fact, these particular worms double their lifespan when you given them a little booze. But “little” is the operative word here: they used ethanol diluted by a factor of 20,000:

“The concentrations correspond to a tablespoon of ethanol in a bathtub full of water or the alcohol in one beer diluted into a hundred gallons of water,” Clarke said.

And more wasn’t better: a little more doesn’t provide any additional lifespan benefits; a lot more produces “harmful neurological effects” and kills them. So the optimal dose is a tiny amount.

What does this mean for humans? Very little, at this point. Still, it’s hard not to compare the results to all the human studies that have found longevity benefits for very moderate amounts of alcohol consumption (i.e. a glass a day), but not for larger amounts. It’s still not clear whether the apparent benefits relate to the ethanol itself, or to all the antioxidants and fancy compounds found in wine (and possibly beer). Could humans be affected by a mechanism similar to what’s going on in these worms?

“While the mechanism of action is still not clearly understood, our evidence indicates that these 1 millimeter–long roundworms could be utilizing ethanol directly as a precursor for biosynthesis of high-energy metabolic intermediates or indirectly as a signal to extend life span. These findings could potentially aid researchers in determining how human physiology is altered to induce cardio-protective and other beneficial effects in response to low alcohol consumption.”

Eventually, your muscles can no longer get enough oxygen. It’s an immutable physical limit that kicks in during any sustained physical exercise and tells your body: “This fast – but no faster.”

At least, that’s the theory we’ve been working with since 1923. But a controversial new study from researchers on three continents suggests that the famous “VO2max” – the maximum amount of oxygen that you’re able to deliver to your muscles during hard exercise – isn’t really a maximum at all. Your heart and lungs don’t call the shots after all; your brain does. [...]

There’s plenty of evidence that lack of sleep puts you at higher risk of gaining weight. A new Swedish study in the Journal of Clinicla Endocrinology and Metabolism (press release here, abstract here) offers some new insights with fMRI brain scans:

We already know that obese people tend to find food more rewarding, as indicated by brain scans of activity in the anterior cingulate cortex:

Higher activation of this brain region has been found in obese compared with normal-weight subjects when anticipating food, suggesting that the rewarding quality of food is enhanced in obesity.

The study took a dozen volunteers and kept them up all night, then looked at their brain’s response to images of food. Compared to after a normal night of sleep, they observed the same changes that you see in obesity: stronger activation of the ACC, indicating higher dopamine signalling. You want more food than normal, because food makes you feel better than it normally would. As the graph on the right shows, those with the biggest changes in brain activity also reported the biggest appetite.

A study like this, where the subjects stayed up all night, isn’t a great way of figuring out what happens in the much more common situation of, say, getting half an hour less sleep than you need, night after night for weeks or months on end. But other studies looking at appetite hormones like ghrelin and leptin suggest that the effects are similar: too little sleep = greater appetite relative to energy needs.

Of course, this leaves us with a riddle: if you have to get up an hour early to fit your workout in, do the benefits outweigh the downsides? That depends on a lot of things, but my general sense is that exercise has so many benefits that it’s still worthwhile. The real answer, of course, is to organize your life so that you can sleep enough and get some exercise.

Very cool new study on massage, from Mark Tarnopolsky’s group at McMaster (abstract here, press release here). Massage is one of those interventions that’s very difficult to study objectively — people like the feel of massage, you can’t blind them, and the outcomes you’re interested in are usually very subjective. But this study does a very good job.

The details: 11 volunteers exercised to exhaustion (about an hour or more on an exercise bike with gradually increasing pace) to induce muscle damage. Then, after a 10-minute break, one of their legs was massaged as follows:

The leg to be massaged was randomly selected, and no one except the massage therapist knew which leg had been massaged until after the results were analyzed.

So how to figure out what the massage did? They took three muscle biopsies from each leg: one at rest, one immediately after the massage, and one 2.5 hours after the massage. Then, because they didn’t know exactly what to expect, they did an untargeted whole-genome analysis to figure out which genes reacted differently between the massaged and non-massaged leg. The result:

[W]hen administered to skeletal muscle that has been acutely damaged through exercise, massage therapy appears to be clinically beneficial by reducing inflammation and promoting mitochondrial biogenesis.

How and why does this happen? The researchers suggest that “mechanical stretch or strain during massage treatment” activates the relevant signalling pathways. In fact, they suggest, the mechanism may be essentially the same as conventional anti-inflammatory drugs. Which is very cool. They also checked the rate of glycogen restoring and lactate clearance in the muscles; neither were improved by massage (which, in the case of lactate, we already knew).

So what does this tell us? Massage does something. Do these acute signalling changes translate to a clinically significant difference in muscle recovery a day later? Impossible to say for now. Is effleurage or petrissage more effective than one of those self-massage devices you can buy from late-night informercials, or than a foam roller? Who knows. But it’s a very good start.

One of the big challenges for researchers trying to figure out how to reduce post-workout muscle soreness is that it’s really hard to quantify that soreness. Asking someone “How sore are you?” is important, but highly susceptible to placebo effects; more objective measures like the enzyme creatine kinase (which is supposed to indicate muscle damage) now tend to be viewed as pretty unreliable proxies for muscle soreness. So how about this:

That’s an image from a new study that used an infrared camera to measure skin temperature before and after a series of biceps curls (press release here; freely available article and video in the Journal of Visualized Experimentshere). They suggest that skin temperature that remains elevated 24 hours after exercise indicate muscle damage:

This damage in the muscle causes additional heat transfer from the muscle to the overlying skin, which causes a detectable hot spot under the skin.

And sure enough, their study did find elevated skin temperature in the biceps (33.96 C instead of 32.80 C) 24 hours after exercise. The problem is that the temperature returned to normal (32.82 C) after 48 hours. The subjects’ subjective assessment of soreness, on the other hand, was equally elevated after 24 and 48 hours — so clearly skin temperature isn’t a perfect proxy for what we experience as soreness. Still, it could be an interesting way for researchers to look at the early stages of delayed-onset muscle soreness in a quantifiable way. And it makes pretty pictures.

Gina Kolata had a New York Times article last week about “brown fat” — the strange, recently discovered (in adult humans, at least) type of fat that burns lots of calories:

A new study finds that one form of it, which is turned on when people get cold, sucks fat out of the rest of the body to fuel itself. Another new study finds that a second form of brown fat can be created from ordinary white fat by exercise.

So what does this mean? No one is really sure at this point, since it’s only been a couple of years since we even realized that it existed in adult humans. Do people become obese because they lack brown fat? Or do they lose brown fat when they become obese? Or does it just seem as if obese people have less brown fat because they don’t get as cold as leaner people, so their brown fat remains dormant? We don’t know.

Still, the article made me think of a pair of posts I wrote last year (here and here) about research that linked the rise in obesity rates with a parallel rise in the typical thermostat settings in U.S. and U.K. homes. Could the warmer ambient temperatures that we expect these days have anything to do with higher rates of obesity? There are many reasons to be highly skeptical about this idea… but the fact that brown fat turns on and starts plowing through calories at colder temperatures does provide a plausible mechanism — beyond shivering — for how temperature could play a role.

Of course, researchers say, they are not blind to the implications of their work. If they could turn on brown fat in people without putting them in cold rooms or making them exercise night and day, they might have a terrific weight loss treatment. And companies are getting to work.

We don’t really need to wait for “companies to get to work,” though. We already know how to trigger brown fat without any pills: even if you don’t go for turning down the thermostat (and I don’t believe there’s anywhere near enough evidence to advise that), the other option — exercise — sounds like a pretty good idea.

Why do you slow down in the heat? This may seem like a painfully obvious question, but it’s a topic of heated (oops) debate among physiologists. There are two basic camps:

You slow down because the increasing temperature in your body begins to cause some sort of physical problem — maybe it’s in your muscles, or your heart, or your nervous system; there are several theories;

You slow down because your brain detects that your body is getting hot, so it forcibly applies the brakes to avoid letting you reach any dangerous system failure (in your muscles, heart, brain, or whatever).

To put it another way, do you slow down in response to problems, or in anticipation of problems?

The problem with many of the experiments on both sides of this debate is that they can’t separate out the conscious psychological factors that also regulate self-paced performance. (I say “self-paced” because that’s what we’re really interested in understanding. Putting someone on a treadmill at a fixed pace and forcing them to run until they fall off is an interesting way of studying our ultimate failure mechanisms, but it offers basically no insight into what happens during a real-life race, where your decision to slow down comes long before you’re at risk of collapsing.)

Anyway, a new study from Stephen Cheung’s group at Brock University, in the journal Physiology & Behavior, takes a clever look at this problem. They told a group of cyclists that they were studying how much power output changes when you try to maintain a constant perceived exertion. To do that, they asked the cyclists to do two 60-minute rides (on separate days) where they maintained their RPE at 14 out of 20 (between somewhat hard and hard). But on the second ride, they secretly manipulated the room temperature as follows:

Now, let’s not kid each other: as the chamber heated up to 35 C, the cyclists knew something was changing. But at this point, they had oxygen tubes in their mouths, and couldn’t communicate with the experimenters. And the point is, they couldn’t consciously regulate their pace in advance to take the hotter temperature into account. Here’s what happened to their power output:

So what’s happening? Well, the power output did go down as they got hotter — but there was no real-time match between power output and any of the other variables that the researchers measured, including skin temperature, rectal temperature, heat storage (a measure of how much thermal energy is accumulating in the body), sweat rate, or heart rate. The verdict seems to be that the brain isn’t using any of these physical cues to anticipatorily regulate power output.

There are some potential limitations to the study — for example, the RPE of 14 might have been too low to cause severe enough thermal stress to trigger a response. But overall, the message seems to be that conscious psychological factors play a role in our response to thermal stress. And that fits with earlier studies like the one I blogged about last May, where lying to cyclists about the temperature allowed them to go just as fast at 31.6 C as they did at 21.8 C. This new study may not support the “anticipatory heat storage” idea of the central governor model, but it certainly reinforces the idea that the brain calls the shots.

A few months ago, I blogged about a placebo-controlled test of the “live high, train low” altitude training paradigm (here, and with a follow-up here). That test found no benefit to altitude training, which prompted some rather heated responses — including a comment from someone who works for an altitude tent company:

One bogus study cannot change the work that guys like David Martin and the Australia of Sport (AIS) have performed.

LHTL, spending at least 14 hours a day for three weeks at simulated 3000 m at the Australian Institute of Sport in Canberra;

a control group that didn’t go to altitude.

To assess the effects of altitude training, they looked at blood parameters like total hemoglobin mass, and measured race performances 1, 7, 14 and 28 days after returning from altitude, as well as assessing season-long performance profiles (including performance at the World Championships).

Let’s start with the good news. Unlike the previous study, this study did find a clear increase in total hemoglobin mass, of about 4%, in both altitude groups. Here’s the individual scatter:

But what about performance? There, the results weren’t so good:

Or in words:

Swimming performance was substantially impaired for up to 7 days following 3 weeks of either Classic or LHTL altitude training. Despite ~4% increases in tHb resulting from both Classic and LHTL altitude training, there were no clear beneficial performance effects in the 28 days following altitude… A season-long comparison of two tapered performances at major championships also did not reveal a benefit for athletes who completed mid-season altitude training despite the substantial physiological changes associated with the altitude.

So does this “prove” that altitude training doesn’t help endurance performance? Of course not. But it’s a pretty interesting data point. This is the Australian swim team — one of the world’s powerhouses — supported by the Australian Institute of Sport, who have done lots of research into altitude training, and believe in it enough to construct an altitude house on their campus. They understand how it’s supposed to be done, and they executed it effectively enough to produce hemoglobin changes… but still, they didn’t manage to improve performance. If anything, they got worse.

If you’re doing altitude training, are you confident that you’re doing it better than they are?

[UPDATE: Sam McGlone and Paulo Sousa raised an important point on Twitter: the swim distances that they tested in this study were 100 or 200m. That's pretty short - I don't know the numbers for swimming, but maybe 50% aerobic at most? Here's what the researchers say:

Based on the calculated aerobic contribution to energy production during competitive 100 and 200 m swimming races, the 3.8% increase in tHb we observed could elicit a 0.3–0.7% improvement in race time... Although improvements of this magnitude are equivalent to the smallest worthwhile change for swimming performance, detecting such changes can be difficult due to the variability associated with racing and the modest sample sizes available when targeting an elite athlete population.

Now the same researchers have published another study, in the current issue of Journal of Strength & Conditioning Research, this time looking at “dynamic” stretching instead of static stretching. Other than the stretching routine, the protocol is exactly the same. The runners spend 15 minutes stretching (or sitting quietly, during the control condition), then run for 30 minutes at 65% VO2max for a running economy measurement, then run as far as they can in the next 30 minutes.

This time, stretching had no significant effect on the distance covered in the time trial: stretchers covered 6.1 +/- 1.3 km, non-stretchers covered 6.3 +/- 1.1 km. On the other hand, the dynamic stretching did increase range of motion in the sit-and-reach test just as much as static stretching (from 32.3 to 37.6 cm). So the basic conclusion: if you’re really into stretching before a run, dynamic stretching will allow you to work on your flexibility without hurting your running performance.

One subtlety, which you pick up if you look at the individual results:

The dynamic warm-up routine takes a fair amount of energy (more details on that below). So you might wonder: for the less fit runners in the group, is it possible that they’re just tired out? The researchers do allude to this possibility:

[I]t is interesting to note that our top 2 performance runners both increased their performance under the dynamic stretching condition with the top runner seeing the largest increase in distance covered in the dynamic stretching condition of 0.2 km. Furthermore, the 2 runners in our study who covered the shortest distance performed better during the nonstretching control condition with the worst performance runner seeing the largest decline in performance after the stretching condition (i.e., 0.6 km). It is possible that elite endurance runners need a warm-up protocol of greater intensity and duration than do recreationally trained runners.

Looking back at the data, it actually looks to me like the top runner was better in the non-stretching condition, but maybe that’s just an artifact of the line thickness they used in the graph. Either way, the differences are pretty small in all cases. To me, the moral of the story is: if you’re an endurance athlete, you may have many reasons for why and how you stretch, but “going faster” shouldn’t be one of them.

As an addendum, here’s the stretching routine the study used:

A total of 10 different movements were used and completed in 15 minutes by performing 2 sets of 4 repetitions of each movement. The dynamic stretching movements were performed in the following order:

(a) Toe and Heel Walks: In these exercises, the subjects walked on their toes for 4 steps followed by walking on their heels for 4 steps to stretch the entire calf complex.

(b) Hip Series: The subjects performed a dynamic stretch of the hip flexors and extensors by placing their hands on a wall with their arms fully extended so that their body was at a 45 angle. In this position, each subject lifted his leg off the ground while bringing the knee to the chest and stepping over a hurdle placed laterally before returning to the starting position.

(c) Hand Walks: The subjects stretched their calves and hamstrings by beginning in a pushup position and walking their feet as close to their hands while keeping their heels flat. As soon as the subjects’ heels came off the ground, they walked with their hands back to a pushup position.

After the hand walks, the subjects performed a series of walking lunges, including (d) rear lunges, (e) lateral lunges, (f ) forward lunges, (g) a knee pull to a lunge, and (h) an ankle pull to a lunge to focus on the quadriceps and gluteus maximus.

(i) Walking Groiners: The subjects began this movement in a pushup position and then brought 1 foot next to the same side hand as to perform a groiner. Instead of holding this position, the subjects walked their hands out to return to the starting position before performing the action on the opposite leg.

(j) Frankensteins: The subjects stood with their feet together and their arms extended straight out in front of them so that their arms were parallel to the ground. While walking, the subjects were instructed to kick 1 leg up to touch the opposite hand to focus on the hamstrings. Every time a step was taken, a kick was made.